title: How does the oxidative burst of macrophages kill bacteria? Still an open question.
abstract: Reactive oxygen species (ROS) are critical components of the antimicrobial repertoire of macrophages, yet the mechanisms by which ROS damage bacteria in the phagosome are unclear. The NADH-dependent phagocytic oxidase produces superoxide, which dismutes to form H(2)O(2). The Barras and Méresse labs use a GFP fusion to an OxyR regulated gene to show that phagocyte-derived H(2)O(2) is gaining access to the Salmonella cytoplasm. However, they have also shown previously that Salmonella has redundant systems to detoxify this H(2)O(2). Although Salmonella propagate in a unique vacuole, their data suggest that ROS are not diminished in this modified phagosome. These recent results are put into the context of our overall understanding of potential oxidative bacterial damage occurring in macrophages.
authors.affiliation: Department of Microbiology, University of Illinois, 601 S Goodwin Ave, Urbana, IL 61801, USA. slauch@illinois.edu
authors.forename: James M
authors.initials: JM
authors.lastname: Slauch
mesh_terms: D006861:Hydrogen Peroxide / Q000378:metabolism / Q000633:toxicity; D008658:Inactivation, Metabolic; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology*; D050296:Microbial Viability / Q000187:drug effects; D008954:Models, Biological; D010588:Phagosomes / Q000378:metabolism / Q000382:microbiology; D017382:Reactive Oxygen Species / Q000378:metabolism / Q000633:toxicity*; D016897:Respiratory Burst; D012475:Salmonella / Q000187:drug effects* / Q000276:immunology* / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D013481:Superoxides; D006861:Hydrogen Peroxide